This project will study the cause(s) of an epidemic in cases of acquired immunodeficiency by several approaches: 1. Substitute cryoprecipitate therapy for commercially obtained factor VIII concentrate in immunologically compromised hemophiliacs. 2. Monitor the effects such therapy has on immunologic markers felt representative of the acquired immunodeficiency syndrome (AIDS). 3. Establish a nonhuman primate model of the AIDS. Our hypothesis is that chronic viral infusions cause the immunodeficiency we have found in hemophiliacs. This will be tested by treating newly diagnosed or multiply treated patients with cryoprecipitate derived from a unique pool of carefully selected donors. Since our preliminary studies suggest that we may quickly segregate those who have impaired immunological defenses for early treatment, this will represent an attempt to reverse the phenotypic abnormalities thought to be important in the development of an acquired immunodeficiency syndrome. Such treatment may have implications for many multiply transfused patients and blood donor populations alike. Parallel, prospective, in vitro studies will determine the extent that lymphocyte subpopulations can be modulated by the mode and intensity of therapy; follow the natural course of these immunologic changes in group of hemophiliacs who receive factor VIII therapy to determine if these observed changes are predictive of those patients who develop the AIDS; investigate the mechanism of the observed abnormalities. A primate model of the AIDS will be established by introducing human factor VIII concentrate into rhesus monkeys. Since workers in our Delta Primate Center have shown that similar immunological markers exist in man and this species of monkey, the early onset and mechanisms of causation of the AIDS will be approached. Viral cultures of the agent causing AIDS from factor concentrate, cryoprecipitate or hemophilic blood will be attempted by these same workers.